1. Many world-class clinicians
state that ME is either an infectious disease, or an auto-immune disease as a
direct result of infectious insult and recognise ME as a complex neuro-immune
disorder accompanied by chronic low-grade inflammation, increased levels of
oxidative and nitrosative stress.(Maes et al 2014), requiring a skilled
biomedical response.

2. ME was recognised as a
specific disease entity by The Royal Society of Medicine in 1978 and by the
World Health Organisation since 1969 as an organic neurological disease, ME is
currently classified under ICD code G93.3. In the USA, ME ranks second only to
HIV as the cause of serious, long-term illness. (Hooper 2004)

3. Cycles of severe relapse are
common, as are further symptoms developing over time. Around 30% of cases are
progressive and degenerative and sometimes ME is fatal. (National CFIDS
Foundation). Two reviews have concluded that, “Substantial improvement is
uncommon and is less than 6%"(Anderson et al. 2004); and "Full
recovery... is rare". (Cairns & Hotopf, 2005)

4. According to the Chief Medical
Officer (DH 2002) people with Severe ME in the UK currently receive
"seriously inadequate health care”.

5. There is a significant body of
compelling published evidence, demonstrating the involvement of the central
nervous system, the autonomic nervous system and the peripheral nervous system
in the pathogenesis of ME, as well as immunological and vascular disruption.
(Williams 2004)

6. There are known to be so many
issues with the body’s defence against pathogens, the Immune System, in ME that
it has also been called CFIDS, Chronic Fatigue and Immune Dysfunction Syndrome.
When the immune system has been seriously disrupted, all kinds of bacteria can
no longer be eliminated.

7. ME is not a somatoform, “all
in the mind”, psychiatric disorder. The documented biochemical, metabolic,
vascular, neurological and muscle abnormalities in ME/CFS patients (Williams
2004) have led to the WHO classification of ME as a neurological illness. The
UK Department of Health and the WHO Collaborating Centre at the Institute of
Psychiatry have agreed that ME is undoubtedly neurological. There is no
published evidence whatsoever, as opposed to opinion, that ME (as distinct from
chronic fatigue) is a psychiatric disorder. (Williams 2004)

8. ME is not ‘medically
unexplained.’ ME is a multi-system disease with many organ and bodily systems
affected, producing a myriad of symptoms [and] many aspects of the
pathophysiology of the disease have, indeed, been medically explained in
volumes of research. (ME Society of America)

9. Cognitive Behaviour Therapy
(CBT) and Graded Exercise Therapy (GET) are potentially harmful to anyone with
ME. The Chief Medical Officer (2002) warned that exercise-based regimes
advocated for less severely affected patients tend not to have been studied
among those most severely affected. Shepherd (2001) warns that as much care
should be taken in prescribing exercise as in prescribing pharmaceuticals, for
ME patients do not respond to exercise in a manner that is expected of healthy
people. (Streeten et al 2001)

10. It is not 'fatigue' or
'tiredness' that is the one essential characteristic of ME/CFS but central
nervous system (CNS) dysfunction (Bassett 2006). As leading ME expert Dr Byron
Hyde MD (2003) explains: “The one essential characteristic of M.E. is acquired
CNS dysfunction, [not] chronic fatigue. A patient with M.E. is a patient whose
primary disease is CNS change, and this is measurable”

11. It has been shown that ME,
alongside a wide range of seemingly unrelated disorders, such as Alzheimer’s,
Diabetes, may have mitochondrial dysfunction in common (Pieczenik and Neustadt
2007); the research appears to be suggesting that blood flow problems are
affecting the mitochondria’s ability to produce energy instead of the
mitochondria themselves being messed up in ME. (Johnson 2013). It has been
estimated that people with ME are about a litre short of blood.

12. Cardiovascular dysfunction in
ME patients has been well documented for many years. (Williams 2008)

13. Cardiac output in normal
people will vary from 7 litres per min to 5 litres per min between standing and
supine. In healthy people this drop is not enough to affect function. But in ME
sufferers Peckerman found that the drop may be from 5 litres lying down to 3.5
litres standing up. At this level, people with ME may be in borderline heart
and organ failure.(Peckerman et al 2003)

14. Studies have shown that the
baroreflex response that regulates blood pressure is under performing,
particularly in Severe ME. (Peckerman et al 2003) The heart’s job is to
maintain blood pressure. If the blood pressure falls, organs start to fail and
are shut down in terms of priority.

15. A study showing that the mean
age of ME patients dying from heart failure is significantly lower than the age
of those dying from heart failure in the general US population, implies that ME
is a risk factor to cardio-vascular disorder.( Maes and Twisk 2009 )

16. Maes et al (2009) found that
Coenzyme Q10 deficiency in ME is related to fatigue, autonomic and
neurocognitive symptoms and is a risk factor explaining the early mortality in
ME due to cardiovascular disorder.

17. Neurocognitive problems,
strikingly similar to those of patients presented with D-lactic acidosis
(linked to Short Bowel Syndrome) reported to be made worse by physical or
mental exertion, are one of the most frequent and disabling symptoms associated
with ME. (Sheedy et al 2009)

18. In 2009 a study found vitamin
D levels to be considerably lower in ME patients than in healthy people. Soon
after an investigation at the University of Dundee discovered an association
between lower vitamin D levels and arterial stiffness, dysfunction of the
endothelium (the lining of blood vessels) and inflammation, in ME patients.
(Breakthrough Spring 2015)

19. ME is not depression.
Research, for example, shows that ME patients show more alpha
electroencephalographic activity during non-REM sleep, but this is not seen in
dysthymic or major depressive disorder (Whelton, Salit, & Moldofsky, 1992).
There are five major clinical tests of depression, all related to disturbances
of the HPA (Hypothalamic-Pituitary-Adrenal) axis; they are, increased levels of
Overnight Cortisol, 24-hour urinary cortisol, Corticotropin-releasing hormone,
Arginine vasopressin and Adrenocorticotropin hormone (ACTH), ACTH is a hormone
that is often released in response to stress, high ACTH levels can be an
indicator of depression. ME patients, generally, show none of these signs, that
is because ME, contrary to what many doctors wrongly believe, is not
depression. (cf. Komaroff 2015)

21. The neurocognitive impairment
in ME has been found to be rooted in physical dysfunction, not maladaptive
thinking, related to decreased cerebral blood flow velocity. (Ocon et al 2011)

22. Hickie (1991) found that
general characteristics of depression: anhedonia (lack of pleasure in life);
weight loss; suicidal ideation; severe psychomotor change; pathological guilt;
and severe anxiety, are not typical in ME.

23. ME is not deconditioning. The
predominant psychiatric paradigm, still seems to be that patients have
medically unexplained chronic fatigue, and that their problems derive from
deconditioning consequent on physical inactivity at best and simple avoidance
behaviour (underpinned by abnormal illness beliefs) at worst. (Scottish Cross
Party Submission 2005).

24. What happens in ME has little
to do with cardiovascular deconditioning (Spence & Stewart 2004) and is
more related to chronic orthostatic intolerance/postural tachycardia syndrome
(POTS), caused by vascular dysfunction.

25. Studies have shown that most
patients do not avoid minimal activity and that lack of fitness is not related
to the fatigue in ME (Bazelmans et al 2001 ). Moreover, deconditioning cannot
explain the documented delay between the end of exertion and the exacerbation
of symptoms, the upregulated immune system etc. (De Merlier et al 2000)

26. Although, as with lupus,
multiple sclerosis and ovarian cancer for example, there is no medical test
available to confirm a diagnosis of ME, it is absurd to claim no objective or
quantifiable abnormalities can be found in patients with Severe ME. (Bassett
2006) “Tests will only all be normal in M.E. patients – as with all illnesses –
if completely the wrong tests are done, or if those tested do not in fact have
M.E. in the first place.” (Bassett 2006)

27. A 2015 study at Stanford
University, comparing brain MRI images, found that the brains of people with ME
differ from healthy subjects in at least three distinct ways: white-mater
content was reduced by about 7%, a consistent abnormality in the right arcuate
fasciculus was identified with links to the severity of illness and there was a
thickening of grey matter, where the two areas of the brain connect at the
right arcuate fasciculus. These results, showing strong evidence for Central
Nervous System defects, were reported widely around the world. (Breakthrough
Spring 2015)

28. Certain aspects of immune
system dysfunction, dysregulation of the RNase L pathway, hyperactive NF-kappaB
leading to disturbed apoptotic mechanisms and oxidative stress or excessive
nitric oxide, for example, appear to be present in both Cancer and in ME and
may play a role in the two diseases and in the physiopathology of the common
symptom fatigue. (Meeus et al 2009)

29. There is evidence that ME is
characterised by increased oxidative stress (Maes et al 2011). Researchers at
the University of Dundee have found that people with ME have high levels of
reactive oxygen molecules which can harm blood vessels and muscles.
(Breakthrough Spring 2015)

30. There is good evidence that
ME patients have a generalised hyperalgesia (an increased sensitivity to pain
throughout the body which increases after stressors and following exercise –
this is unusual because sensitivity to pain normally decreases in people during
physical activity. (Breakthrough Spring 2012)

31. Problems with eyes and vision
are common feature of ME, including eye pain (which is severe or very severe in
one third of cases), prominent eye movement dysfunction and visual processing
issues. (ME Research 2015)

32. Studies examining the
microecology of the gastrointestinal (GI) tract have identified specific
microorganisms whose presence appears related to ME, which is associated with
marked alterations in the gut microbiota, with lower levels of Bifidobacteria
and higher levels of aerobic bacteria. A CFIDS Association of America pilot
study, for example, found greatly increased ratios of Firmicute/Bacteriodetes
bacteria before and after exercise in ME. (CIFDS 2013)

33. It has been found that a
significant subset of ME patients may have a chronic, non-cytolytic form of
enteroviral infection which could be diagnosed by stomach biopsy. (Chia 2008)

34. Reports also suggest that ME
patients may have a major drop in all E.Coli species - in contrast to Crohn’s
Disease where over 95% of the invasive species are E.Coli. (Lassesen 2013)

35. One of the most consistently
observed abnormalites in ME is hypocortisolism (low cortisol levels); there is
evidence for reduced cortisol and ACTH production/responsiveness in ME,
alongside evidence of reduced adrenal gland productivity. A mutation in the
cortisol binding globulin gene (CBG) has also been found in people with ME,
this impaired CBG functioning would exacerbate any cortisol deficiencies
already present. (Torpy et. al. 2001)

36. New Scientist magazine
reported in July 2015 that nearly two thirds of people, diagnosed with “ME/CFS”
who have taken Rituximab, a drug normally used to knock out white blood cells
in people with lymphoma and rheumatoid arthritis, have experienced a major remission
of their symptoms. We are not sure, however, if Rituximab really is a potential
treatment for ME; it could be that the two thirds of patients it helped have
“CFS”, not ME, for “ME/CFS” is an umbrella term, subject to many different
interpretations, incorporating a wide range of meaning and poorly identified
conditions. If you have ME, caused by an enterovirus, the John Richardson Group
(2013) warn, it could be very dangerous indeed to take Rituximab, which
suppresses the immune/virus balance.

It should be stressed that any registered medical practitioner,
consultant or GP, in the UK, who chooses to dismiss or ignore widely available
biomedical evidence for ME, may be in breach of the legal requirement for
doctors to keep up to date with developments in medicine and medical science
and this consequently raises issues of medical indemnity.(Hooper 2010 )

In the UK, there is no act of parliament setting out patient’s rights,
however the NHS must take account of law made by parliament (e.g. Human Rights
Act etc.) or by court judgements. Health professionals must use reasonable care
and skill and patients are entitled to receive care of a standard which a
“responsible body of medical opinion” considers to be appropriate to their
condition. If the duty of care is breached, the patient may be able to sue for
negligence.(NHS 2006)

About Me

I am a Christian, saved by grace alone through faith alone. I have had the neuroimmune disorder ME, Myalgic Encephalomyelitis, since 1991. From North Somerset, now in N. Ireland. Please see my website for further information about ME.